Biomedical subjects
Publications and source records attributed to R Korbut.
Myricetin at a dose of 3.6 micrograms/kg iv was found to inhibit the cat blood platelet aggregation in vivo. It disaggregated platelet thrombi in vitro at a concentration of 60 nM. This flavonoid bound to platelet membranes and prevented prostacyclin synthase against oxygen free radicals owing to its antioxidant properties. Myricetin inhibited soybean lipoxygenase when linoleic acid was used as a substrate.
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Properties of several products of cyclo-oxygenation of polyunsaturated fatty acids: prostacyclin, prostaglandins 6-keto E1, E2, D2, D3 are reviewed in relation to their antiplatelet activity.
The mechanism of antiplatelet potency of prostanoids and pharmacological methods that regulate their endogenous release are discussed. In addition the role of antiaggregatory prostanoids in atherosclerosis and some clinical trials with prostanoids are reviewed.
We have shown that streptokinase (SK) is capable of building up thrombi in vivo on the blood-superfused collagen strips in extracorporal circulation of anaesthetized cats. The thrombogenic effects of SK appeared in all animals, irrespectively of whether SK was administered as intravenous bolus injections or infusions at doses comparable to those used for the treatment of patients with acute myocardial infarction. The thrombogenic phase of SK lasted up to 1.5 h and was followed by expected thrombolytic phase. Both phases were mediated by generation of plasmin. Inhibition of cyclooxygenase by aspirin or nitric oxide synthase by NG-nitro-L-arginine did not prevent SK from being thrombogenic. Also nitric oxide donor-SIN-1 did not remove the formation of thrombi by SK. The only effective treatment consisted of complementing the SK therapy with exogenous prostacyclin-like activity (e.g. iloprost). Prostacyclin not only abolishes thrombogenesis by SK but it also intensifies its thrombolytic action.